The data of this study suggested that point contacts are a targeted site of local translation within growth cones, and RACK1 is a critical member of the point contact complex and necessary for appropriate neural development.

A sequential and coordinated activation of ERK, JNK and STAT3 with RACK1 is shown to accelerate aggressive melanoma development in vivo.

Leads to the enhanced and previously un-described interaction of RACK1 and TCTP.

urther investigation indicated that p205 may disturb the formation of Runx2/Ids complex and free more Runx2 to induce the differentiation process. Taken together, our findings demonstrated for the first time that p205 functions as an activator in osteoblast differentiation.

RACK1 competes with Rab40C for binding to the ANKR2 domain of Varp and regulates dendrite outgrowth through stabilization of Varp in mouse melanocytes

Rack1/PI3K/Rac1 signaling pathway may play a crucial role in malignant biological behaviors of mouse hepatocarcinoma cells with lymphatic metastasis potential

The results suggest RACK1 as a downstream target gene of TGF-beta1 involved in the modulation of liver fibrosis progression in vitro and in vivo, and propose a strategy to target RACK1 for liver fibrosis treatment.

findings demonstrate that RACK1 is involved in p300/GATA4-dependent hypertrophic responses in cardiomyocytes and is a promising therapeutic target for heart failure

RACK1 may alleviate the severity of acute pancreatitis.

High RACK1 expression is associated with Hepatocellular Carcinoma.

These results suggest that RACK1 promotes cell growth and invasion and inhibits the senescence and apoptosis in cervical cancer cells probably by affecting the p53 pathway.

The present findings indicate that RACK1 silencing attenuates renal fibrosis by suppressing the activation of TGF-beta1/Smad3 signaling pathway in HK-2 cells. Thus, RACK1 may serve as a novel regulator of renal fibrosis.

RACK1 associates with MOAP-1 via electrostatic associations similar to those observed between MOAP-1/RASSF1A and MOAP-1/TNF-R1. These events illustrate the complex nature of MOAP-1 regulation and characterizes the important role of the scaffolding protein, RACK1, in influencing MOAP-1 biology.

data provided evidence that increased Rack1-mediated upregulation of PKC kinase activity may be responsible for the development of chemoresistance in T-ALL-derived cell line potentially by reducing FEM1b and Apaf-1 level.

the depletion of ribosomal RACK1 alters the capacity of the ribosome to translate specific mRNAs, resulting in selective translation of mRNAs of genes for non-canonical autophagy induction.

This work has significantly advanced our understanding of the RACK1/PP2A complex and suggests a pro-carcinogenic role for the RACK1/PP2A interaction. This work suggests that approaches to target the RACK1/PP2A complex are a viable option to regulate PP2A activity and identifies a novel potential therapeutic target in the treatment of breast cancer.

Our analysis shows that most of the interaction partners with putative regulatory functions have binding sites that are available on ribosomal RACK1, supporting the role of RACK1 as a ribosomal signaling hub.

This supports PDE4D5 and RACK1 as potential regulators of cell adhesion, spreading and migration through the non-classical exchange protein activated by cyclic AMP (EPAC1)/Rap1 signalling route

In this review we summarize this evidence and examine the mechanisms that underlie the contribution of RACK1 to the various stages of cell migration and invasion.

Analysis of deletion constructs of SERBP1 showed that the C-terminal third of the SERBP1 protein, which contains one of its two substrate sites for protein arginine N-methyltransferase 1 (PRMT1), is necessary and sufficient for it to interact with RACK1

identification of regulatory elements in the promoter of RACK1 shed some light on its transcriptional modulation in physiological and pathological context.These and other informations suggest that a better understanding of RACK1 transcriptional regulation is essential to unravel its role.

Data indicate that OR3A4 upregulation contributes to metastasis and tumorigenesis in gastric cancer by regulating the activation of PDLIM2, MACC1, NTN4, and GNB2L1.

High RACK1 expression is associated with imatinib resistance in gastrointestinal stromal tumor.

The upregulation of RACK1 can promote the proliferation and invasion of nasopharyngeal carcinoma by regulating the PI3K/Akt/FAK signal pathway.

It has been found that the adaptor protein receptor for activated PKC kinase (RACK1) formed a complex with FGFR1 and PKM2, and activated the FGFR1/PKM2 signaling. The study shows that RACK1 forms a complex with FGFR1 and PKM2, and stimulates the growth and migration of squamous lung cancer cells.

GNB2L1 and its O-GlcNAcylation regulated metastasis via modulating the translation of epithelial-mesenchymal transition-related proteins in the chemoresistance of gastric cancer.